Alzheimer's disease term paper

Not mentioned is Aluminium. Aluminum, Al is implicated in neurofibrillary tangles, NFT, ie the death of the neuron in the brain, that leading to dementia, Alzheimers, and seizures. The science shows that Al. plays a role in NFT formation by acting on the tau protein, the major component of NFTs. Studies associate Al with abnormal fetal neurologilcal development, then in the growing child, Al is associated with bone deformation, as the bone growth is disrupted. In the adult, as well as the effects on the brain, there is difficulty in fracture healing, immune suppresion, muscle weakness chronic fatigue, and pain in the bones. Studies also confirm confirm that high doses of Al induce toxic effects and damage the lysosomes in the liver, the spleen and the kidneys. While Al is plentiful in nature, where it is bound with other compounds for easy excretion by the kidneys, in its pure form, it rapidly builds up and is stored, as the kidneys do not have the ability to excrete the larger amounts. Aluminium comes from cookware, foils, food packaging, pre-cooked foods and soy isolates. Its alos in vax., anti-acid tablets, and is in nearly all toothpaste, (unmarked because its 'natural'!)!

People with memory loss or other possible signs of Alzheimer’s may find it hard to recognize they have a problem. Signs of dementia may be more obvious to family members or friends. Anyone experiencing dementia-like symptoms should see a doctor as soon as possible. If you need assistance finding a doctor with experience evaluating memory problems, your local Alzheimer's Association chapter can help. Early diagnosis and intervention methods are improving dramatically, and treatment options and sources of support can improve quality of life. Two helpful support resources you can tap into are ALZConnected , our messages boards and online social networking community, and Alzheimer's Navigator , a web tool that creates customized action plans, based on answers you provide through short, online surveys.

Most cases of Alzheimer's disease do not exhibit autosomal-dominant inheritance and are termed sporadic AD, in which environmental and genetic differences may act as risk factors . The best known genetic risk factor is the inheritance of the ε4 allele of the apolipoprotein E (APOE). [45] [46] Between 40 and 80% of people with AD possess at least one APOEε4 allele. [46] The APOEε4 allele increases the risk of the disease by three times in heterozygotes and by 15 times in homozygotes. [40] Like many human diseases, environmental effects and genetic modifiers result in incomplete penetrance . For example, certain Nigerian populations do not show the relationship between dose of APOEε4 and incidence or age-of-onset for Alzheimer's disease seen in other human populations. [47] [48] Early attempts to screen up to 400 candidate genes for association with late-onset sporadic AD (LOAD) resulted in a low yield. [40] [41] More recent genome-wide association studies (GWAS) have found 19 areas in genes that appear to affect the risk. [49] These genes include: CASS4 , CELF1 , FERMT2 , HLA-DRB5 , INPP5D , MEF2C , NME8 , PTK2B , SORL1 , ZCWPW1 , SlC24A4 , CLU , PICALM , CR1 , BIN1 , MS4A , ABCA7 , EPHA1 , and CD2AP . [49]